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Global Initiative for Chronic

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Obstructive

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Lung

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Disease

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POCKET GUIDE
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TO COPD DIAGNOSIS, MANAGEMENT,

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AND PREVENTION
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A Guide for Health Care Professionals

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U P D AT ED 2 0 10
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Global Initiative for Chronic

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Obstructive
L ung

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Disease

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OR
Pocket Guide to COPD Diagnosis, Management,
and Prevention

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GOLD Ex ecu t iv e Co m m it t ee TA
Roberto Rodriguez-Roisin, MD, Spain, Chair
Antonio Anzueto, MD, US (representing ATS)
Jean Bourbeau, MD, Canada
NO

Teresita S. DeGuia, MD, Philippines

David Hui, MD, Hong Kong, ROC
O

Christine Jenkins, MD, Australia

-D

Fernando Martinez, MD, US

Michiaki Mishima, MD, Japan (representing APSR)
María Montes de Oca, MD, PhD (representing ALAT)
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Robert Stockley, MD, UK

Chris van Weel, MD, Netherlands (representing WONCA)
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Jorgen Vestbo, MD, Denmark

Ob s er v er :
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Jadwiga Wedzicha, MD, UK (Representing ERS)

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GOLD Nat io n al L ead er s

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Representatives from many countries serve as a network for the dissemination and
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implementation of programs for diagnosis, management, and prevention of COPD.

The GOLD Executive Committee is grateful to the many GOLD National Leaders who
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participated in discussions of concepts that appear in GOLD reports, and for their
comments during the review of the 2006 Global Strategy for the Diagnosis,
Management, and Prevention of COPD.
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© 2010 Global Initiative for Chronic Obstructive Lung Disease, Inc.

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TA B L E O F CON T EN T S

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3 P R EFA CE

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5 K EY P O I N T S
6 W H AT I S CH R O N I C OB S T R U CT I V E

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P U L M ON A R Y D I S EA S E ( CO P D ) ?
7 R I S K FA CT OR S : WH AT CA U S ES CO P D ?

OR
8 D I A GN O S I N G COP D
Figure 1: Key Indicators for Considering a
COPD Diagnosis

ER
Figure 2: Normal Spirogram and Spirogram Typical of
Patients with Mild to Moderate COPD

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Figure 3: Differential Diagnosis of COPD
12 CO M P ON EN T S OF CA R E: TA
A COP D M A N A G EM EN T P R O GR A M
13 Co m p o n e n t 1 : A s s e s s a n d M o n i t o r D i s e a s e
15 Co m p o n e n t 2 : R e d u ce R i s k F a ct o r s
NO

Figure 4: Strategy to Help a Patient Quit Smoking

17 Co m p o n e n t 3 : M a n a g e S t a b l e COP D
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Patient Education
Pharmacologic Treatment
-D

Figure 5: Commonly Used Formulations of Drugs for COPD

Non-Pharmacologic Treatment
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Figure 6: Therapy at Each Stage of COPD

22 Co m p o n e n t 4 : M a n a g e Ex a ce r b a t i o n s
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How to Assess the Severity of an Exacerbation

Home Management
Hospital Management
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Figure 7: Indications for Hospital Admission

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for Exacerbations
24 A P P EN D I X I : S P I R OM ET R Y F OR D I A G N OS I S OF COP D
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PREFACE

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Chronic Obstructive Pulmonary Disease (COPD) is a major cause of

RE
chronic morbidity and mortality throughout the world. The Globa l
In it iat iv e f or Ch ro n ic Ob s t r u ct iv e L u n g Dis eas e was created to
increase awareness of COPD among health professionals, public health

OR
authorities, and the general public, and to improve prevention and
management through a concerted worldwide effort. The Initiative
prepares scientific reports on COPD, encourages dissemination and

ER
adoption of the reports, and promotes international collaboration on
COPD research.

LT
TA
While COPD has been recognized for many years, public health officials
are concerned about continuing increases in its prevalence and mortality,
which are due in large part to the increasing use of tobacco products
NO

worldwide and the changing age structure of populations in developing

countries. The Global In it iat iv e f or Ch r on ic Obs t r u ct iv e L u n g
Dis eas e offers a framework for management of COPD that can be
O

adapted to local health care systems and resources. Educational tools,

-D

such as laminated cards or computer-based learning programs, can be

prepared that are tailored to these systems and resources.
IAL

The Glob al In it iat iv e f or Ch r on ic Ob s t r u ct iv e L u n g Dis eas e

ER

program includes the following publications:

• Global Strategy for the Diagnosis, Management, and Prevention of
T

COPD. Scientific information and recommendations for COPD

MA

programs. (Updated 2010)

• Executive Summary, Global Strategy for the Diagnosis, Management,
D

and Prevention of COPD. (Updated 2010)

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• Pocket Guide to COPD Diagnosis, Management, and Prevention.

Summary of patient care information for primary health care
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professionals. (Updated 2010)

• What You and Your Family Can Do About COPD. Information booklet
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for patients and their families.

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These publications are available on the Internet at www.goldcopd.org.

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This site provides links to other websites with information about COPD.

This Pocket Guide has been developed from the Global Strategy for the

PR
Diagnosis, Management, and Prevention of COPD (2010). Technical
discussions of COPD and COPD management, evidence levels, and specific

RE
citations from the scientific literature are included in that source document.

OR
A ck n o w l e d g e m e n t s : Grateful acknowledgement is given for the educational
grants from Almirall, AstraZeneca, Boehringer Ingelheim, Chiesi, Dey, Forest
Laboratories, GlaxoSmithKline, Novartis, Nycomed, Pfizer, Philips Respironics, and

ER
Schering-Plough. The generous contributions of these companies assured that the
participants could meet together and publications could be printed for wide distribu-

LT
tion. The participants, however, are solely responsible for the statements and con-
clusions in the publications. TA
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KEY POINTS

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PR
• Ch r o n i c O b s t r u ct i v e P u l m o n a r y D i s e a s e ( COP D ) is a
preventable and treatable disease with some significant extra-

RE
pulmonary effects that may contribute to the severity in individual
patients. Its pulmonary component is characterized by airflow limitation
that is not fully reversible. The airflow limitation is usually progressive

OR
and associated with an abnormal inflammatory response of the lung
to noxious particles or gases.

ER
• Worldwide, the most commonly encountered r i s k f a ct o r for COPD
is ci g a r e t t e s m o k i n g . A t e v e r y p o s s i b l e o p p o r t u n i t y

LT
i n d i v i d u a l s w h o s m o k e s h o u l d b e e n co u r a g e d t o q u i t . In
TA
many countries, air pollution resulting from the burning of wood and
other biomass fuels has also been identified as a COPD risk factor.
NO

• A d i a g n o s i s of COPD should be considered in any patient who has

dyspnea, chronic cough or sputum production, and/or a history of
exposure to risk factors for the disease. The diagnosis should be
O

confirmed by spirometry.
-D

• A CO P D m a n a g e m e n t p r o g r a m includes four components:

IAL

assess and monitor disease, reduce risk factors, manage stable

COPD, and manage exacerbations.
ER

• P h a r m a co l o g i c t r e a t m e n t can prevent and control symptoms,

reduce the frequency and severity of exacerbations, improve health
T

status, and improve exercise tolerance.

MA

• P a t i e n t e d u ca t i o n can help improve skills, ability to cope with

illness, and health status. It is an effective way to accomplish smoking
D

cessation, initiate discussions and understanding of advance directives

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and end-of-life issues, and improve responses to acute exacerbations.

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• COPD is often associated with e x a ce r b a t i o n s of symptoms.

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WHAT IS CHRONIC

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OBSTRUCTIVE

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PULMONARY DISEASE

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(COPD)?

OR
Ch r o n i c Ob s t r u ct i v e P u l m o n a r y D i s e a s e ( CO P D ) is a preventable

ER
and treatable disease with some significant extrapulmonary effects that may
contribute to the severity in individual patients. Its pulmonary component
is characterized by airflow limitation that is not fully reversible. The air-

LT
flow limitation is usually progressive and associated with an abnormal
TA
inflammatory response of the lung to noxious particles or gases.

This definition does not use the terms chronic bronchitis and emphysema*
NO

and excludes asthma (reversible airflow limitation).

S y m p t o m s o f CO P D i n cl u d e :
O
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• Cough
• Sputum production
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• Dyspnea on exertion
ER

Episodes of acute worsening of these symptoms often occur.

T
MA

Ch r o n i c co u g h a n d s p u t u m p r o d u ct i o n o f t e n p r e ce d e t h e
d e v e l o p m e n t o f a i r f l o w l i m i t a t io n b y m a n y y e a r s , a l t h o u g h
n o t a l l i n d i v i d u a l s w i t h co u g h a n d s p u t u m p r o d u ct i o n g o o n
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t o d e v e l o p COP D .
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*Chronic bronchitis, defined as the presence of cough and sputum production for at least 3
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months in each of 2 consecutive years, is not necessarily associated with airflow limitation.
Emphysema, defined as destruction of the alveoli, is a pathological term that is sometimes
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(incorrectly) used clinically and describes only one of several structural abnormalities present
in patients with COPD.
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RISK FACTORS:

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WHAT CAUSES COPD?

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Wo r l d w i d e , ci g a r e t t e s m o k i n g i s t h e m o s t co m m o n l y

RE
e n co u n t e r e d r i s k f a ct o r f o r CO P D .

The genetic risk factor that is best documented is a severe hereditary

OR
deficiency of alpha-1 antitrypsin. It provides a model for how other
genetic risk factors are thought to contribute to COPD.

ER
COPD risk is related to the total burden of inhaled particles a person
encounters over their lifetime:

LT
• To b a cco s m o k e , including cigarette, pipe, cigar, and other types
TA
of tobacco smoking popular in many countries, as well as
environmental tobacco smoke (ETS)
NO

• Occu p a t i o n a l d u s t s a n d ch e m i ca l s (vapors, irritants, and

fumes) when the exposures are sufficiently intense or prolonged
• I n d o o r a i r p o l l u t i o n from biomass fuel used for cooking and
O

heating in poorly vented dwellings, a risk factor that particularly

-D

affects women in developing countries

• Ou t d o o r a i r p o l l u t i o n also contributes to the lungs’ total burden
IAL

of inhaled particles, although it appears to have a relatively small

effect in causing COPD
ER

In addition, any factor that affects lung growth during gestation and
childhood (low birth weight, respiratory infections, etc.) has the potential
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for increasing an individual’s risk of developing COPD.

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DIAGNOSING

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COPD

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A diagnosis of COPD should be considered in any patient who has dyspnea,

RE
chronic cough or sputum production, and/or a history of exposure to risk
factors for the disease, especially cigarette smoking (FF i g u r e 1 ).

OR
F i g u r e 1 : K e y I n d i ca t o r s f o r Co n s id e r i n g a COP D D i a g n o s i s

ER
Consider COPD, and perform spirometry, if any of these indicators
are present in an individual over age 40. These indicators are not

LT
diagnostic themselves, but the presence of multiple key indicators
increases the probability of a diagnosis of COPD.
TA
• D y s p n e a that is: Progressive (worsens over time).
Usually worse with exercise.
NO

Persistent (present every day).

Described by the patient as an “increased
effort to breathe,” “heaviness,” “air hunger,”
O

or “gasping.”
-D

• Ch r o n ic co u g h : May be intermittent and may be unproductive.

• Ch r o n ic s p u t u m p r o d u ct i o n :
Any pattern of chronic sputum production may
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indicate COPD.
• H i s t o r y o f e x p o s u r e t o r i s k f a ct o r s :
To b a cco s m o k e ( in cl u d in g p o p u l a r l o ca l
ER

p r e p a r a t io n s ) .
Occupational dusts and chemicals.
T

Smoke from home cooking and heating fuel.

MA

T h e d i a g n o s i s s h o u l d b e co n f i r m e d b y s p i r o m e t r y *
D

( F i g u r e 2 , p a g e 9 a n d A p p e n d i x I, p a g e 2 4 ) .
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*Where spirometry is unavailable, the diagnosis of COPD should be made using all
available tools. Clinical symptoms and signs (abnormal shortness of breath and increased
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forced expiratory time) can be used to help with the diagnosis. A low peak flow is consistent
with COPD but has poor specificity since it can be caused by other lung diseases and by
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poor performance. In the interest of improving the accuracy of a diagnosis of COPD, every
effort should be made to provide access to standardized spirometry.
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When performing spirometry, measure:

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• F orced V ital Capacity (FF V C) and
• F orced Expiratory V olume in one second (FF EV 1 ).

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Calculate the FEV1/FVC ratio.

RE
Spirometric results are expressed as % P r e d i ct e d using
appropriate normal values for the person’s sex, age, and height.

OR
F i g u r e 2 : N o r m a l S p i r o g r a m a n d S p i r o g r a m Ty p i ca l o f

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P a t i e n t s w i t h M i l d t o M o d e r a t e CO P D *

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TA
NO
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*Postbronchodilator FEV1 is recommended for the diagnosis

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and assessment of severity of COPD.

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P a t i e n t s w i t h COP D t y p ica l l y s h o w a d e cr e a s e in b o t h F EV 1
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a n d F EV 1 /F V C. T h e d e g r e e o f s p i r o m e t r ic a b n o r m a l i t y
g e n e r a l l y r e f l e ct s t h e s e v e r i t y o f COP D . H o w e v e r, b o t h
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s y m p t o m s a n d s p ir o m e t r y s h o u l d b e c o n s i d e r e d w h e n
d e v e l o p in g a n i n d i v id u a l i z e d m a n a g e m e n t s t r a t e g y f o r
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e a ch p a t i e n t .
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St a g es o f COP D

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St a ge I: Mild COP D - Mild airflow limitation (FEV1/FVC < 70%;
FEV1 ≥ 80% predicted) and sometimes, but not always, chronic cough

PR
and sputum production.

RE
• At this stage, the individual may not be aware that his or her lung
function is abnormal.

OR
St a ge II: Mo de r at e COP D - Worsening airflow limitation
(FEV1/FVC < 70%; 50% ≤ FEV1 < 80% predicted), with shortness

ER
of breath typically developing on exertion.

• This is the stage at which patients typically seek medical attention

LT
because of chronic respiratory symptoms or an exacerbation of their
disease.
TA
St a ge III: Sev er e COP D - Further worsening of airflow limitation
NO

(FEV1/FVC < 70%; 30% ≤ FEV1 < 50% predicted), greater shortness of
breath, reduced exercise capacity, and repeated exacerbations which
have an impact on patients’ quality of life.
O
-D

St a ge IV: Ver y Sev e r e COP D - Severe airflow limitation

(FEV1/FVC < 70%; FEV1 < 30% predicted) or FEV1 < 50% predicted
plus chronic respiratory failure. Patients may have Very Severe (Stage IV)
IAL

COPD even if the FEV1 is > 30% predicted, whenever this complication
is present.
ER

• At this stage, quality of life is very appreciably impaired and

T

exacerbations may be life-threatening.

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“ At R is k f or COP D”
D

A major objective of GOLD is to increase awareness among health care providers and the
TE

general public of the significance of COPD symptoms. The classification of severity of COPD
now includes four stages classified by spirometry—Stage I: Mild COPD; Stage II: Moderate
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COPD; Stage III: Severe COPD; Stage IV: Very Severe COPD. A fifth category—“Stage 0: At
Risk”—that appeared in the 2001 report is no longer included as a stage of COPD, as there
is incomplete evidence that the individuals who meet the definition of “At Risk” (chronic cough
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and sputum production, normal spirometry) necessarily progress on to Stage I: Mild COPD.
Nevertheless, the importance of the public health message that chronic cough and sputum are
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D if f e r e n t ia l D i a g n o s i s : A major differential diagnosis is asthma. In

OD
some patients with chronic asthma, a clear distinction from COPD is not
possible using current imaging and physiological testing techniques. In these
patients, current management is similar to that of asthma. Other potential

PR
diagnoses are usually easier to distinguish from COPD (FF ig u r e 3 ).

RE
F i g u r e 3 : D i f f e r e n t i a l D i a g n o s i s o f CO P D

OR
D ia g n o s is Su g g e s t iv e Fe a t u r e s *
COPD Onset in mid-life.

ER
Symptoms slowly progressive.
Long smoking history.
Dyspnea during exercise.

LT
Largely irreversible airflow limitation.
Asthma Onset early in life (often childhood).
TA
Symptoms vary from day to day.
Symptoms at night/early morning.
Allergy, rhinitis, and/or eczema also present.
NO

Family history of asthma.

Largely reversible airflow limitation.
Congestive Heart Failure Fine basilar crackles on auscultation.
O

Chest X-ray shows dilated heart, pulmonary edema.

-D

Pulmonary function tests indicate volume restriction, not airflow

limitation.
Bronchiectasis Large volumes of purulent sputum.
IAL

Commonly associated with bacterial infection.

Coarse crackles/clubbing on auscultation.
ER

Chest X-ray/CT shows bronchial dilation, bronchial wall thickening.

Tuberculosis Onset all ages.
Chest X-ray shows lung infiltrate or nodular lesions.
T

Microbiological confirmation.
MA

High local prevalence of tuberculosis.

Obliterative Bronchiolitis Onset in younger age, nonsmokers.
May have history of rheumatoid arthritis or fume exposure.
D

CT on expiration shows hypodense areas.

TE

Diffuse Panbronchiolitis Most patients are male and nonsmokers.

Almost all have chronic sinusitis.
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Chest X-ray and HRCT show diffuse small centrilobular

nodular opacities and hyperinflation.
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*These features tend to be characteristic of the respective diseases, but do not occur in
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every case. For example, a person who has never smoked may develop COPD (especially
in the developing world, where other risk factors may be more important than cigarette
smoking); asthma may develop in adult and even elderly patients.
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COMPONENTS OF CARE:

OD
A COPD MANAGEMENT

PR
PROGRAM

RE
OR
The goals of COPD management include:

ER
• Relieve symptoms
• Prevent disease progression
• Improve exercise tolerance

LT
• Improve health status TA
• Prevent and treat complications
• Prevent and treat exacerbations
• Reduce mortality
NO

• Prevent or minimize side effects from treatment

Cessation of cigarette smoking should be included as a goal throughout

O

the management program.

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T H ES E G OA L S CA N B E A CH I EV ED T H R OU G H
I M P L EM EN TAT I ON OF A COP D M A N A GEM EN T P R OG R A M
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WI T H F OU R COM P O N EN T S :
ER

1 . A s s e s s a n d M o n it o r D is e a s e

2 . R e d u ce R i s k F a ct o r s
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3 . M a n a g e S t a b l e CO P D

4 . M a n a g e Ex a c e r b a t i o n s
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Component 1: Assess and Monitor Disease

OD
A d e t a i l e d m e d i ca l h i s t o r y of a new patient known or thought to

PR
have COPD should assess:

RE
• Exposure to risk factors, including intensity and duration.

OR
• Past medical history, including asthma, allergy, sinusitis or nasal
polyps, respiratory infections in childhood, and other respiratory
diseases.

ER
• Family history of COPD or other chronic respiratory disease.

LT
• Pattern of symptom development. TA
• History of exacerbations or previous hospitalizations for
respiratory disorder.
NO

• Presence of comorbidities, such as heart disease, malignancies,

osteoporosis, and musculoskeletal disorders, which may also
O

contribute to restriction of activity.

-D

• Appropriateness of current medical treatments.

IAL

• Impact of disease on patient’s life, including limitation of activity;

missed work and economic impact; effect on family routines; and
ER

feelings of depression or anxiety.

T

• Social and family support available to the patient.

MA

• Possibilities for reducing risk factors, especially smoking cessation.

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In addition to s piro m e t r y , the following ot h er t es t s may be considered
for the assessment of a patient with Moderate (Stage II), Severe

OD
(Stage III), and Very Severe (Stage IV) COPD.

PR
• B ro n ch od ilat o r r e v er s ibilit y t e s t in g: To rule out a diagnosis of
asthma, particularly in patients with an atypical history (e.g., asthma

RE
in childhood and regular night waking with cough and wheeze).

• Ch es t X - r a y : Seldom diagnostic in COPD but valuable to exclude

OR
alternative diagnoses such as pulmonary tuberculosis, and identify
comorbidities such as cardiac failure.

ER
• Ar t er ia l blo od ga s m ea s u r em e n t : Perform in patients with

LT
FEV1 < 50% predicted or with clinical signs suggestive of respiratory
failure or right heart failure. The major clinical sign of respiratory
TA
failure is cyanosis. Clinical signs of right heart failure include ankle
edema and an increase in the jugular venous pressure. Respiratory
failure is indicated by PaO2 < 8.0 kPa (60 mm Hg), with or without
NO

PaCO2 > 6.7 kPa (50 mm Hg) while breathing air at sea level.
O

• Alph a - 1 an t it r y p s in def icie n cy s cr een in g: Perform when

-D

COPD develops in patients of Caucasian descent under 45 years or

with a strong family history of COPD.
IAL
T ER
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COP D is u s u ally a p ro g r es s iv e dis ea s e. L u n g f u n ct io n

ca n b e ex pect ed t o w o r s en o v er t im e, ev en w it h t h e b es t
av aila ble car e. Sy m p t o m s a n d lu n g f u n ct io n s h o u ld be
D

m o n it o r ed t o f o llo w t h e d ev elo p m en t o f co m plica t ion s , t o

TE

gu ide t r ea t m en t , an d t o f acilit a te d is cu s s io n o f m an a gem en t

o pt io n s w it h pa t ien t s . Co m o r bidit ies a r e co m m o n in COP D
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an d s h o u ld b e a ct iv ely id en t if ied .
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Component 2: Reduce Risk Factors

OD
S m o k i n g ce s s a t i o n i s t h e s i n g l e m o s t e f f e ct i v e —a n d co s t -
e f f e ct i v e —i n t e r v e n t i o n t o r e d u ce t h e r i s k o f d e v e l o p i n g

PR
COP D a n d s l o w i t s p r o g r e s s i o n .

RE
• Even a brief, 3-minute period of counseling to urge a smoker to
quit can be effective, and at a minimum this should be done for
every smoker at every health care provider visit. More intensive

OR
strategies increase the likelihood of sustained quitting (FF i g u r e 4 ).

ER
• Pharmacotherapy (nicotine replacement, buproprion/nortryptiline,
and/or varenicline) is recommended when counseling is not sufficient
to help patients stop smoking. Special consideration should be

LT
given before using pharmacotherapy in people smoking fewer than
TA
10 cigarettes per day, pregnant women, adolescents, and those
with medical contraindications (unstable coronary artery disease,
untreated peptic ulcer, and recent myocardial infarction or stroke
NO

for nicotine replacement; and history of seizures for buproprion).

O

F ig u r e 4 : S t r a t e g y t o H e l p a P a t ie n t Qu it Sm o k in g
-D

1. A S K : Systematically identify all tobacco users at every visit.

Implement an office-wide system that ensures that, for EVERY patient
IAL

at EVERY clinic visit, tobacco-use status is queried and documented.

2. A D V I S E: Strongly urge all tobacco users to quit.
ER

In a clear, strong, and personalized manner, urge every tobacco user

to quit.
T

3. A S S ES S : Determine willingness to make a quit attempt.

MA

Ask every tobacco user if he or she is willing to make a quit attempt

at this time (e.g., within the next 30 days).
4. A S S I S T: Aid the patient in quitting.
D

Help the patient with a quit plan; provide practical counseling;

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provide intra-treatment social support; help the patient obtain

extra-treatment social support; recommend use of approved
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pharmacotherapy if appropriate; provide supplementary materials.

5. A R R A NG E: Schedule follow-up contact.
Schedule follow-up contact, either in person or via telephone.
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S m o k i n g P r e v e n t i o n : Encourage comprehensive tobacco-control

OD
policies and programs with clear, consistent, and repeated nonsmoking
messages. Work with government officials to pass legislation to establish
smoke-free schools, public facilities, and work environments and

PR
encourage patients to keep smoke-free homes.

RE
Occu p a t i o n a l Ex p o s u r e s : Emphasize primary prevention, which
is best achieved by elimination or reduction of exposures to various
substances in the workplace. Secondary prevention, achieved through

OR
surveillance and early detection, is also important.

ER
I n d o o r a n d O u t d o o r A i r P o l l u t i o n : Implement measures to reduce
or avoid indoor air pollution from biomass fuel, burned for cooking and
heating in poorly ventilated dwellings. Advise patients to monitor public

LT
announcements of air quality and, depending on the severity of their
TA
disease, avoid vigorous exercise outdoors or stay indoors altogether
during pollution episodes.
NO
O
-D
IAL
T ER
MA
D
TE
GH
RI
PY
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Component 3: Manage Stable COPD

OD
M a n a g e m e n t o f s t a b l e CO P D s h o u l d b e g u i d e d b y t h e
f o l l o w i n g g e n e r a l p r i n ci p l e s :

PR
• Determine disease severity on an individual basis by taking into

RE
account the patient’s symptoms, airflow limitation, frequency and
severity of exacerbations, complications, respiratory failure,
comorbidities, and general health status.

OR
• Implement a stepwise treatment plan that reflects this assessment of
disease severity.

ER
• Choose treatments according to national and cultural preferences,
the patient’s skills and preferences, and the local availability of
medications.

LT
P a t i e n t e d u ca t i o n can help improve skills, ability to cope with illness,
TA
and health status. It is an effective way to accomplish smoking cessation,
initiate discussions and understanding of advance directives and end-of-
NO

life issues, and improve responses to acute exacerbations.

P h a r m a co l o g i c t r e a t m e n t (FF i g u r e 5 ) can control and prevent

O

symptoms, reduce the frequency and severity of exacerbations, improve

-D

health status, and improve exercise tolerance.

B r o n ch o d i l a t o r s : These medications are central to symptom

IAL

management in COPD.
ER

• Inhaled therapy is preferred.

• Give “as needed” to relieve intermittent or worsening symptoms, and
T

on a regular basis to prevent or reduce persistent symptoms.

MA

• The choice between ␤2-agonists, anticholinergics, methylxanthines,

and combination therapy depends on the availability of medications
and each patient’s individual response in terms of both symptom
D

relief and side effects.

TE

• Regular treatment with long-acting bronchodilators, including nebu-

lized formulations, is more effective and convenient than treatment
GH

with short-acting bronchodilators.

• Combining bronchodilators of different pharmacologic classes may
RI

improve efficacy and decrease the risk of side effects compared to

increasing the dose of a single bronchodilator.
PY
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Figure 5. Formulations and Typical Doses of COPD Medications*
Drug Inhaler Solution for Oral Vials for Duration of

OD
(µg) Nebulizer Injection Action (hours)
(mg/ml) (mg)

PR
β2-agonists
Short-acting

RE
Fenoterol 100-200 (MDI) 1 0.05% (Syrup) 4-6
Levalbuterol 45-90 (MDI) 0.21, 0.42 6-8
Salbutamol (albuterol) 100, 200 (MDI & DPI) 5 5mg (Pill), 0.024%(Syrup) 0.1, 0.5 4-6

OR
Terbutaline 400, 500 (DPI) 2.5, 5 (Pill) 4-6
Long-acting
Formoterol 4.5-12 (MDI & DPI) 0.01± 12+

ER
Arformoterol 0.0075 12+
Indacaterol 150-300 (DPI) 24
Salmeterol 25-50 (MDI & DPI) 12+

LT
Anticholinergics TA
Short-acting
Ipratropium bromide 20, 40 (MDI) 0.25-0.5 6-8
Oxitropium bromide 100 (MDI) 1.5 7-9
NO

Long-acting
Tiotropium 18 (DPI), 5 (SMI) 24+
Combination short-acting β2-agonists plus anticholinergic in one inhaler
O

Fenoterol/Ipratropium 200/80 (MDI) 1.25/0.5 6-8

-D

Salbutamol/Ipratropium 75/15 (MDI) 0.75/0.5 6-8

Methylxanthines
IAL

Aminophylline 200-600 mg (Pill) 240 mg Variable, up to 24

Theophylline (SR) 100-600 mg (Pill) Variable, up to 24
Inhaled glucocorticosteroids
ER

Beclomethasone 50-400 (MDI & DPI) 0.2-0.4

Budesonide 100, 200, 400 (DPI) 0.20. 0.25, 0.5
T

Fluticasone propionate 50-500 (MDI & DPI)

MA

Combination long-acting β2-agonists plus glucocorticosteroids in one inhaler

Formoterol/Budesonide 4.5/160, 9/320 (DPI)
Salmeterol/Fluticasone 50/100, 250. 500 (DPI)
D

propionate 25/50, 125, 250 (MDI)

Systemic glucocorticosteroids
TE

Prednisone 5-60 mg (Pill)

GH

Methyl-prednisolone 4, 8, 16 mg (Pill)
Phosphodiesterase-4 inhibitors
Roflumilast 500 mcg (Pill) 24
RI

MDI=metered dose inhaler; DPI=dry powder inhaler

PY

*Not all formulations are available in all countries; in some countries, other formulations may be available.
±Formoterol nebulized solution is based on the unit dose vial containing 20 µgm in a volume of 2.0ml
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Inhaled Glucocorticosteroids: Regular treatment with inhaled
glucocorticosteroids does not modify the long-term decline in FEV1 but

OD
has been shown to reduce the frequency of exacerbations and thus
improve health status for symptomatic patients with an FEV1 < 50%
predicted and repeated exacerbations (for example, 3 in the last three

PR
years). The dose-response relationships and long-term safety of inhaled
glucocorticosteroids in COPD are not known. Treatment with inhaled glu-

RE
cocorticosteroids increases the likelihood of pneumonia and does not
reduce overall mortality.

OR
An inhaled glucocorticosteroid combined with a long-acting β2-agonist is
more effective than the individual components in reducing exacerbations
and improving lung function and health status. Combination therapy

ER
increases the likelihood of pneumonia and has no significant effects on
mortality. In patients with an FEV1 less than 60%, pharmacotherapy with

LT
long-acting β2-agonist, inhaled glucocorticosteroid and its combination
decreases the rate of decline of lung function. Addition of a long-acting
TA
β2-agonist/inhaled glucocorticosteroid to an anticholinergic (tiotropium)
appears to provide additional benefits.
NO

Oral Glucocorticosteroids: Long-term treatment with oral glucocorticosteroids

is not recommended.
O

Phosphodiesterase-4 inhibitors: In patients with Stage III: Severe COPD or

Stage IV: Very Severe COPD and a history of exacerbations and chronic
-D

bronchitis, the phosphodiesterase-4 inhibitor, roflumilast, reduces exacerba-

tions treated with oral glucocorticosteroids. These effects are also seen
IAL

when roflumilast is added to long-acting bronchodilators; there are no

comparison studies with inhaled glucocorticosteroids.
ER

Vaccines: Influenza vaccines reduce serious illness and death in COPD

patients by 50%. Vaccines containing killed or live, inactivated viruses
T

are recommended, and should be given once each year. Pneumococcal

MA

polysaccharide vaccine is recommended for COPD patients 65 years and

older, and has been shown to reduce community-acquired pneumonia in
those under age 65 with FEV1 < 40% predicted.
D
TE

An t ibiot ics : Not recommended except for treatment of infectious

exacerbations and other bacterial infections.
GH

M u co ly t ic (Mu co k in et ic, Mu cor e gu lat or ) Agen t s: Patients with

viscous sputum may benefit from mucolytics, but overall benefits are very
RI

small. Use is not recommended.

PY

An t it u s siv e s: Regular use contraindicated in stable COPD.

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Non - P h ar m acolo gic Tr e at m en t includes rehabilitation, oxygen
therapy, and surgical interventions.

OD
Rehabilitation: Patients at all stages of disease benefit from exercise
training programs improvements in exercise tolerance and symptoms of

PR
dyspnea and fatigue. Benefits can be sustained even after a single pulmo-
nary rehabilitation program. The minimum length of an effective rehabili-

RE
tation program is 6 weeks; the longer the program continues, the more
effective the results. Benefit does wane after a rehabilitation program
ends, but if exercise training is maintained at home the patient's health

OR
status remains above pre-rehabilitation levels.

Th e go a ls of pu lm on a r y r eh ab ilit at io n a r e t o r ed u ce s y m pt o m s ,

ER
im pr o v e qu a lit y o f life, a n d in cr ea s e pa r t icipa t io n in ev er y da y
a ct iv itaties
Patients all. stages of disease benefit from exercise training programs,

LT
Ox y gen Th e r apy : The long-term administration of oxygen (>15 hours
TA
per day) to patients with chronic respiratory failure increases survival and
has a beneficial impact on pulmonary hemodynamics, hematologic
NO

characteristics, exercise capacity, lung mechanics, and mental state.

Initiate oxygen therapy for patients with Stage IV: Very Severe COPD if:
O

• PaO2 is at or below 7.3 kPa (55 mm Hg) or SaO2 is at or below

-D

88%, with or without hypercapnia; or

• PO2 is between 7.3 kPa (55 mm Hg) and 8.0 kPa (60 mm Hg)
IAL

or SaO2 is 88%, if there is evidence of pulmonary hypertension,

peripheral edema suggesting congestive heart failure, or
polycythemia (hematocrit > 55%).
T ER

Th e go a l o f lo n g- t er m o x y gen t h er a py is t o in cr ea s e t h e ba s e-
MA

lin e P a O2 a t r es t t o a t lea s t 8.0 k P a (60 m m Hg) a t s ea lev el,

a n d/o r pr o du ce Sa O2 a t lea s t 90% , w h ich w ill p r es er v e v it al
o r ga n f u n ct io n b y en s u r in g an ad equ at e d eliv er y of o x y gen .
D
TE

Su r gical Tr e at m en t s : Bullectomy and lung transplantation may be

considered in carefully selected patients with Stage IV: Very Severe
GH

COPD. There is currently no sufficient evidence that would support the

widespread use of lung volume reduction surgery (LVRS).
RI
PY

Th er e is n o con v in cin g ev iden ce t h at m ech an ical v en t ilat or y

su ppor t h as a role in t h e rou tin e m an agem en t of stable COP D.
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A summary of characteristics and recommended treatment at each stage

OD
of COPD is shown in F i g u r e 6 .

PR
Figure 6: Therapy at Each Stage of COPD*

RE
I: Mild II: Moderate III: Severe IV: Very Severe

OR
• FEV1/FVC < 0.70

ER
• FEV1/FVC < 0.70 • FEV1 < 30% predicted
or FEV1 < 50%
• FEV1/FVC < 0.70 predicted plus chronic

LT
respiratory failure
• FEV1/FVC < 0.70 • 30% ≤ FEV1 < 50%

• 50% ≤ FEV1 < 80% predicted

TA
• FEV1 ≥ 8 0% predicted predicted

Active reduction of risk factor(s); influenza vaccination

NO

Add short-acting bronchodilator (when needed)

Add regular treatment with one or more long-acting bronchodilators

O

(when needed); Add rehabilitation

-D

Add inhaled glucocorticosteroids if

repeated exacerbations
IAL

Add long term oxygen if

chronic respiratory
failure
ER

Consider surgical
treatments
T
MA

*Postbronchodilator FEV1 is recommended for the diagnosis and

D

assessment of severity of COPD.

TE
GH
RI
PY
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Component 4: Manage Exacerbations

OD
An exacerbation of COPD is defined as a n e v e n t in t h e n a t u r a l
co u r s e o f t h e d i s e a s e ch a r a ct e r i z e d b y a ch a n g e i n t h e

PR
p a t i e n t ’s b a s e l i n e d y s p n e a , co u g h , a n d /o r s p u t u m t h a t i s
b e y o n d n o r m a l d a y - t o - d a y v a r i a t i o n s , i s a cu t e i n o n s e t ,

RE
a n d m a y w a r r a n t a ch a n g e i n r e g u l a r m e d i ca t i o n i n a
p a t i e n t w i t h u n d e r l y i n g CO P D .

OR
The most common causes of an exacerbation are infection of the
tracheobronchial tree and air pollution, but the cause of about one-third

ER
of severe exacerbations cannot be identified.

LT
H o w t o A s s e s s t h e S e v e r i t y o f a n Ex a ce r b a t i o n
TA
Arterial blood gas measurements (in hospital):
NO

• PaO2 < 8.0 kPa (60 mm Hg) and/or SaO2 < 90% with or without
PaCO2 > 6.7 kPa, (50 mmHg) when breathing room air indicates
O

respiratory failure.
-D

• Moderate-to-severe acidosis (pH < 7.36) plus hypercapnia (PaCO2

> 6-8 kPa, 45-60 mm Hg) in a patient with respiratory failure is an
IAL

indication for mechanical ventilation.

Chest X-ray: Chest radiographs (posterior/anterior plus lateral) identify

ER

alternative diagnoses that can mimic the symptoms of an exacerbation.

T

ECG: Aids in the diagnosis of right ventricular hypertrophy, arrhythmias,

MA

and ischemic episodes.

Other laboratory tests:

D

• Sputum culture and antibiogram to identify infection if there is

TE

no response to initial antibiotic treatment.

GH

• Biochemical tests to detect electrolyte disturbances, diabetes,

and poor nutrition.
RI

• Whole blood count can identify polycythemia or bleeding.

PY
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Hom e Car e o r Ho s pit al Car e f o r En d - St a ge COP D P at ien t s ?

OD
Th e r is k of dy in g f ro m a n ex acer ba t io n o f COP D is clos ely r ela t ed
t o t h e dev elo p m en t o f r es pir a t o r y acido s is , t h e p r es en ce o f
s er iou s com o r b idit ies , a n d t h e n eed f o r v en t ila t o r y s u pp o r t .

PR
P at ien t s lack in g t h es e f eat u r es a r e n o t at h igh r is k o f dy in g , bu t
t h o s e w it h s ev er e u n der ly in g COP D o f ten r eq u ir e h o s p ita lizat io n
in a n y ca s e. At t em p t s at m a n ag in g s u ch p at ien t s en t ir ely in t h e

RE
co m m u n it y h av e m et w it h lim it ed s u cces s , b u t r et u r n in g t h em
t o t h eir h om es w it h in cr ea s ed s o cia l s u p po r t an d a s u p er v is ed
m edica l car e p ro g r am af t er an in it ia l em er gen cy r o om as s es s m en t

OR
h as b een m u ch m o r e s u cces s f u l. Ho w ev er, d et ailed co s t - ben ef it
a n a ly s es o f t h es e ap p ro a ch es h av e n o t b een r ep o r t ed .

ER
H om e Ma n age m e n t
B ron ch odila t o r s: Increase dose and/or frequency of existing short-

LT
acting bronchodilator therapy, preferably with 2-agonists. If not already
used, add anticholinergics until symptoms improve.
TA
Glu cocor t ico st er oids : If baseline FEV1 < 50% predicted, add 30-40
mg oral prednisolone per day for 7-10 days to the bronchodilator regimen.
NO

Budesonide alone may be an alternative to oral glucocorticosteroids in the

treatment of exacerbations and is associated with significant reduction
of complications.
O

H os pit a l Man agem en t

-D

Patients with the characteristics listed in Figu r e 7 should be hospitalized.

Indications for referral and the management of exacerbations of COPD
IAL

in the hospital depend on local resources and the facilities of the local
hospital.
ER

Figu r e 7: In dica t io n s fo r Ho s pit al Adm is s ion fo r Ex acerb at ion s

• Marked increase in intensity of • Failure of exacerbation to respond
T

symptoms, such as sudden develop- to initial medical management

MA

ment of resting dyspnea • Significant comorbidities

• Severe underlying COPD • Frequent exacerbations
• Onset of new physical signs (e.g., • Newly occurring arrhythmias
D

cyanosis, peripheral edema) • Diagnostic uncertainty

TE

• Older age
• Insufficient home support
GH

An t ibio t ics: Antibiotics should be given to patients:

• With the following three cardinal symptoms: increased dyspnea,
RI

increased sputum volume, increased sputum purulence

PY

• With increased sputum purulence and one other cardinal symptom

• Who require mechanical ventilation
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APPENDIX I:

OD
SPIROMETRY FOR

PR
DIAGNOSIS OF COPD

RE
Spirometry is as important for the diagnosis of COPD as blood

OR
pressure measurements are for the diagnosis of hypertension.
Spirometry should be available to all health care professionals.

ER
Wh a t is S p i r o m e t r y ?

LT
S p i r o m e t r y is a simple test to measure the amount of air a
person can breathe out, and the amount of time taken to do so.
TA
A s p i r o m e t e r is a device used to measure how effectively, and
how quickly, the lungs can be emptied.
NO

A s p i r o g r a m is a volume-time curve.
O

Spirometry measurements used for diagnosis of COPD include

(see Figure 2, page 9):
-D

• F V C (Forced Vital Capacity): maximum volume of air that

IAL

can be exhaled during a forced maneuver.

ER

• F EV 1 (Forced Expired Volume in one second): volume expired in

the first second of maximal expiration after a maximal inspiration.
This is a measure of how quickly the lungs can be emptied.
T
MA

• F EV 1/F V C: FEV1 expressed as a percentage of the FVC,

gives a clinically useful index of airflow limitation.
D

The ratio FEV1/FVC is between 70% and 80% in normal adults; a

TE

value less than 70% indicates airflow limitation and the possibility
GH

of COPD.

FEV1 is influenced by the age, sex, height and ethnicity, and is

RI

best considered as a percentage of the predicted normal value.

PY

There is a vast literature on normal values; those appropriate for

local populations should be used1,2,3.
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W h y d o S p i r o m e t r y f o r CO P D ?

OD
• Spirometry is needed to make a firm diagnosis of COPD.

PR
• Together with the presence of symptoms, spirometry helps stage
COPD severity and can be a guide to specific treatment steps.

RE
• A normal value for spirometry effectively excludes the diagnosis
of clinically relevant COPD.

OR
• The lower the percentage predicted FEV1, the worse the
subsequent prognosis.

ER
• FEV1 declines over time and faster in COPD than in healthy
subjects. Spirometry can be used to monitor disease progres-
sion, but to be reliable the intervals between measurements must

LT
be at least 12 months. TA
W h a t Yo u N e e d t o P e r f o r m S p i r o m e t r y
NO

Several types of spirometers are available:

O

• relatively large bellows or rolling-seal spirometers (usually only

-D

available in pulmonary function laboratories). Calibration

should be checked against a known volume e.g. from a 3-litre
syringe on a regular basis.
IAL

• smaller hand-held devices, often with electronic calibration

ER

systems.

A hard copy of the volume time plot is very useful to check

T

optimal performance and interpretation, and to exclude errors.

MA

Most spirometers require electrical power to permit operation of

D

the motor and/or sensors. Some battery operated versions are

available that can dock with a computer to provide hard copy.
TE
GH
RI
PY
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I t i s e s s e n t i a l t o l e a r n h o w y o u r m a ch i n e i s ca l i b r a t e d

OD
a n d w h e n a n d h o w t o cl e a n i t .

PR
H o w t o P e r f o r m S p ir o m e t r y
Spirometry is best performed with the patient seated. Patients may

RE
be anxious about performing the tests properly, and should be
reassured. Careful explanation of the test, accompanied by a

OR
demonstration, is very useful. The patient should:
• Breathe in fully.

ER
• Seal their lips around the mouthpiece.
• Force the air out of the chest as hard and fast as they can

LT
until their lungs are completely “empty.” TA
• Breathe in again and relax.
NO

Exhalation must continue until no more air can be exhaled, must

be at least 6 seconds, and can take up to 15 seconds or more.
O

Like any test, spirometry results will only be of value if the

-D

expirations are performed satisfactorily and consistently. Both

FVC and FEV1 should be the largest value obtained from any of
3 technically satisfactory curves and the FVC and FEV1 values in
IAL

these three curves should vary by no more than 5% or 100 ml,

whichever is greater. The FEV1/FVC is calculated using the maxi-
ER

mum FEV1 and FVC from technically acceptable (not necessarily

the same) curves.
T
MA

Those with chest pain or frequent cough may be unable to

perform a satisfactory test and this should be noted.
D
TE
GH
RI
PY
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Wh e r e t o f in d m o r e d e t a i l e d i n f o r m a t i o n o n

OD
s p ir o m e t r y
1 . A m e r i ca n T h o r a ci c S o ci e t y

PR
http://www.thoracic.org/adobe/statements/spirometry1-30.pdf

RE
2. A u s t r a l i a n /N e w Z e a l a n d T h o r a ci c S o ci e t y
http://www.nationalasthma.org.au/publications/spiro/index.htm

OR
3. B r i t i s h T h o r a ci c S o ci e t y
http://www.brit-thoracic.org.uk/copd/consortium.html

ER
4. G O L D
A spirometry guide for general practitioners and a teaching slide

LT
set is available:
http://www.goldcopd.org TA
NO
O
-D
IAL
T ER
MA
D
TE
GH
RI
PY
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27
28
CO
PY
RI
GH
TE
D
NOTES
MA
TER
IAL
-D
O
NO
TA
LT
ER
OR
RE
PR
OD
UC
E
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The Global Initiative for Chronic Obstructive Lung Disease
is supported by unrestricted educational grants from:

OD
PR
RE
OR
ER
LT
TA
NO
O
-D
IAL
T ER
MA
D
TE
GH
RI
PY
CO

Visit the GOLD website at www.goldcopd.org